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Flashcards in Renal Random Facts Deck (87):
1

What does the mesonephros become?

Men- Wolffian ducts (ductus deferens and epidydimus); Women- vestigal Gartner's duct

2

What is a multi cystic dysplastic kidney

Due to abnormal interaction between ureteric bud and metanephric mesenchyme. Leads to a nonfunctional kidney consisting of cysts and connective tissue

3

Relationship to ureter to ductus deferens

Ureters pass under the ductus deferens

4

What do the uterine vessels travel in?

Cardinal ligament

5

What is the 60-40-20 rule?

60% total body water: 40% intracellular, 20% ECF

6

How do you measure plasma volume and extracellular volume?

Plasma volume measured by radio labeled albumin, extracellular volume measured by inulin

7

Equation for renal blood flow

RBF=RPF/(1-Hct); RPF is the clearance of PAH

8

How does changing the plasma protein concentration change the GFR, RPF, and FF?

Increased plasma protein concentration decreases the GFR, doesn't affect the RPF, and therefore decreases the FF (GFR/RPF)

9

Hartnup disease

Autosomal recessive, deficiency of neutral amino acid transporters in proximal renal tubular cells and on enterocytes, causes a neutral aminoaciduria and decreased absorption from the gut

10

What is Fanconi syndrome

Generalized reabsorptive defect in PCT, associated with increased excretion of nearly all amino acids, glucose, HCO3-, and PO4(3-). May result in metabolic acidosis (proximal renal tubular acidosis)

11

Bartter syndrome

AR, affects Na/K/2Cl transporter, results in hypokalemia and metabolic alkalosis with hypercalciuria

12

Gitelman syndrome

AR, reabsorptive defect of NaCl in DCT. Leads to hypokalemia, hypomagnesemia, metabolic alkalosis, hypocalciuria

13

Liddle syndrome

AD, Gain of function mutation causing increased Na reabsorption in collecting tubules (increased activity of epithelial Na channel). Results in hypertension, hypokalemia, metabolic alkalosis, decreased aldosterone. Tx: amiloride

14

Syndrome of apparent mineralocorticoid excess

Hereditary deficiency of 11-beta-hydroxysteroid dehydrogenase, which normally converts cortisol into cortisone in mineralocorticoid receptor containing cells before cortisol can act on the mineralocorticoid receptors. Causes hypertension, hypokalemia, metabolic alkalosis. Low serum aldosterone levels.

15

Actions of angiotensin II (6)

1. acts at ATII receptors on vascular SM to cause vasoconstriction, 2. Constricts effect arteriole of glomerulus, 3. Increases aldosterone, 4. Stimulates ADH leading to H2O reabsorption, 5. Increases PCT Na/H activity, 6. Stimulates the hypothalamus (thirst)

16

How does the macula densa work?

Senses decreased NaCl deliver to DCT causes adenosine release, causes vasoconstriction

17

Where does Epo come from?

Interstitial cells in peritubular capillary bed

18

Where is vitamin D converted to its active form?

By the PCT cells

19

What do ADH and aldosterone regulate?

ADH regulates osmolarity, aldosterone regulares ECF volume and Na content

20

Effect of ANP

Causes increased GFR and increased Na filtration with NO compensatory Na reabsorption in distal nephron. Net effect: Na loss and volume loss

21

What causes K to shift out of cells?

Digitalis, hyperosmolarity, lysis of cells, acidosis, beta-blocker, high blood sugar (insulin deficiency) [DO LABS}

22

How do you monitor for too much magnesium?

DTRS (hypermagnesemia decreases DTRs), also causes lethargy, bradycardia, hypotension, cardiac arrest, and hypocalcemia

23

Respiratory compensation for metabolic acidosis

Winters formula. Pco2= 1.5[HCO3-] +8 +/-2

24

What can cause a metabolic alkalosis?

Loop/thiazide diuretics, vomiting, antacid use, hyperaldosteronism

25

What causes an anion gap metabolic acidosis?

MUDPILES: methanol, uremia, diabetic ketoacidosis, propylene glycol, iron tablets/isoniazid, lactic acidosis, ethylene glycol (oxalic acid), salicylates

26

What causes a normal anion gap metabolic acidosis?

HARD-ASS: hyperalimentation, addison disease, renal tubular acidosis, diarrhea, acetazolamide, spironolactone, saline infusion

27

Type 1 renal tubular acidosis

Distal, urine pH >5.5, defect in ability of alpha-intercalated cells to secrete H+ -> no new HCO3- is generated -> metabolic acidosis. Associated with hypokalemia, increased risk for calcium phosphate kidney stones (due to increased urine pH and increased bone turnover)

28

Type 2 RTA

Proximal, urine pH

29

Causes of type 2 RTA

Fanconi syndrome and carbonic anhydrase inhibitors

30

Causes of type 1 RTA

Amphotericin B toxicity, analgesic nephropathy, congenital anomalies (obstruction) of urinary tract

31

Type IV RTA

Hyperkalemic, urine pH

32

What causes type IV RTA?

Decreased aldosterone production (e.g. diabetic hyporeninism, ACE inhibitors, ARBs, NSAIDs, heparin, cyclosporine, adrenal insufficiency), or aldosterone resistance (e.g. K-sparing diuretics, nephropathy due to obstruction, TMP/SMX)

33

When do you see waxy casts?

End-stage renal disease/chronic renal failure

34

"Starry sky" granular appearance on light microscopy, "lumpy bumpy"

Acute poststreptococcal glomerulonephritis

35

Where are the immune complex deposits in APGN?

Subepithelial

36

Most impt prognostic factor for APGN?

Age

37

What do the crescents in RPGN consist of?

Fibrin and plasma proteins (ex. C3b) with glomerular parietal cells, monocytes, and macrophages

38

What diseases can lead to RPGN and what do you see with each of them?

Goodpasture- type II hypersensitivity, Ab to GBM, linear immunofluorescence; Granulomatosis with polyangiitis (Wegener)- PR3-ANC/c-ANCA; microscopic polyangiitis- MPO-ANCA, p-ANCA

39

What causes diffuse proliferative glomerulonephritis?

SLE or membranoproliferative glomerulonephritis

40

"Wire looping" of capillaries

DPGN

41

Where are the immune complex deposits in DPGN?

Subendothelial

42

What do you see in IgA nephropathy?

LM-mesangial proliferation; EM-mesangial IC deposits; IF- IgA based IC deposits in mesangium

43

What causes Alport syndrome?

Mutation in type IV collagen, causes thinning and splitting of glomerular basement membrane. Most commonly X-linked

44

"Basket weave" appearance on EM

Alport Syndrome

45

Sx of Alport syndrome

Eye problems, glomerulonephritis, sensorineural deafness

46

Where are the immune complex deposits in type I membranoproliferative glomerulonephritis?

Supendothelial

47

"Tram track" appearance on PAS and H&E stain

MPGN; Due to GBM splitting by mesangial ingrowth

48

Where are the immune complexes in type II MPGN?

Intramembranous

49

What are type I and type II MPGN associated with?

Type I may be 2/2 hepatitis B or C infection. Type II is associated with C3 nephritis factor (stabilizes C3 convertase causing decreased serum C3 levels)

50

Fatty casts

Nephrotic syndrome

51

Most common cause of nephrotic syndrome in AA and hispanics

FSGS

52

Most common cause of nephrotic syndrome in Caucasians

Membranous nephropathy

53

Where are the deposits in Membranous nephropathy?

Subepithelial

54

EM of membranous nephropathy

"Spike and dome" appearance with subepithelial deposits

55

Nephrotic presentation of SLE

Membranous nephropathy

56

LM of membranous nephropathy

granular

57

Diabetic glomerulonephropathy on LM

Mesangial expansion, GBM thickening, eosinophilic nodular glomerulosclerosis (Kimmelstiel-Wilson lesions)

58

How does diabetes cause kidney problems

Non-enzymatic glycosylation of GBM causes increased permeability and thickening; non-enzymatic glycosylation of efferent arterioles causes increased GFR causes mesangial expansion

59

Envelope shaped kidney stone

Calcium oxalate

60

Coffin lid shaped kidney stone

Ammonium magnesium phosphate (aka struvite)

61

Rhomboid or rosette shaped kidney stone

Uric acid

62

Hexagonal kidney stone

Cysteine

63

What is the test for cysteine stones?

Sodium cyanide nitroprusside test

64

Where does renal cell carcinoma arise from?

PCT cells

65

What paraneoplastic syndromes is RCC associated with?

Ectopic EPO, ACTH, PTHrP

66

Large eosinophilic cells with abundant mitochondria without perinuclear clearing

Renal oncocytoma, benign epithelial cell tumor

67

Cause of Wilms tumor

"Loss of function" mutation of tumor suppressor genes WT1 or WT2 on chromosome 11

68

What is Wilms tumor associated with?

Beckwith-Wiedmann: Wilms tumor, macroglossia, organomegaly, hemihypertrophy; WAGR: Wilms, aniridia, genitourinary malformation, mental retardation

69

CT findings in acute pyelonephritis

Striated parenchymal enhancement

70

Thyroidization of the kidney

Chronic pyelonephritis

71

Bone changes with renal osteodystrophy

Subperiosteal thinning of bones

72

What is ARPCD associated with?

Hepatic fibrosis

73

What is medullary cystic disease?

Inherited disease causing tubulointerstitial fibrosis and progressive renal insufficiency with inability to concentrate urine. Medullary cysts usually not visualized; shrunken kidney on ultrasound. Poor prognosis

74

When is mannitol contraindicated?

Anuria, HF

75

Clinical uses for acetazolamide

Glaucoma, urinary alkalinization, metabolic alkalosis, altitude sickness, pseudotumor cerebri

76

Toxicity of acetazolamide

Hyperchloremic metabolic acidosis, paresthesias, NH3 toxicity, sulfa allergy

77

Toxicity of loop diuretics

Ototoxicity, hypokalemia, dehydration, allergy (sulfa), interstitial nephritis, gout

78

Which loop diuretic can be used in patients with a sulfa allergy?

Ethacrynic acid

79

Toxicity of thiazides

HYPER problems: hyperuricemia, hypercalcemia, hyperglycemia, hyperlipidemia; HYPO problems: hypokalemia, hypotension

80

What are the K sparing diuretics

Spironolactone and eplerenone; triamterene, and amiloride

81

MOA of spironolactone and eplerenone

Aldosterone receptor antagonists in cortical collecting tubule

82

MOA of triamterene and amiloride

Block Na channels in the cortical collecting tubule

83

Toxicity of ACE inhibitors

Cough, Angioedema (contraindicated in C1 esterase inhibitor deficiency), Teratogen (fetal renal malformations), increased Creatinine, Hyperkalemia, and Hypotension (especially watch for first dose hypotension)

84

Which drug is a direct renin inhibitor?

Aliskiren

85

When is Aliskiren contraindicated

In diabetics taking ACE inhibitors or ARBs

86

Which diuretics lead to acidemia and how?

Carbonic anhydrase inhibitors: decrease HCO3 reabsorption; K sparing: aldosterone blockade prevents K secretion and H secretion. Additionally, hyperkalemia leads to K entering all cells (via H/K exchanger) in exchange for H exiting cells

87

Which diuretics lead to alkalemia and how

Loop diuretic and thiazides. Volume contraction increases AT II, increases Na/H exchange in PCT, increased HCO3 reabsorption. K loss leads to K exiting all cells (in exchange for H entering cells). In low K state, H (rather than K) is exchanged for Na in cortical collecting tubule causing alkalosis and "paradoxical aciduria"